Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Methcathinone intoxication in the rat: abrogation by dextrorphan

R W Rockhold1, F B Carlton, R Corkern

  • 1Department of Emergency Medicine, University of Mississippi Medical Center, Jackson.

Annals of Emergency Medicine
|March 1, 1997
PubMed
Summary

Dextrorphan effectively counteracts acute methcathinone toxicity in rats by blocking excitatory amino acid receptors. This treatment reduces hyperthermia and tachycardia, and increases lethal doses, minimizing intoxication effects.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Homeopathy a Applied to Veterinary Medicine.

The Journal of comparative medicine and veterinary archives·2022
Same author

Changes in the brain kappa-opioid receptor levels of rats in withdrawal from physical dependence upon butorphanol.

Neuroscience·2003
Same author

Fire ant venom alkaloid, isosolenopsin A, a potent and selective inhibitor of neuronal nitric oxide synthase.

International journal of toxicology·2003
Same author

Focal kappa-opioid receptor-mediated dependence and withdrawal in the nucleus paragigantocellularis.

Pharmacology, biochemistry, and behavior·2002
Same author

Effects of single or repeated dermal exposure to methyl parathion on behavior and blood cholinesterase activity in rats.

Journal of biomedical science·2001
Same author

The bispectral index monitor: a new tool for air medical personnel.

Air medical journal·2001

Area of Science:

  • Neuropharmacology
  • Toxicology
  • Drug Abuse Research

Background:

  • Methcathinone is a designer drug with significant abuse potential.
  • Acute toxicity of methcathinone presents serious health risks.

Purpose of the Study:

  • To characterize the acute toxicity of methcathinone in a rat model.
  • To investigate the potential of dextrorphan, an excitatory amino acid receptor antagonist, in mitigating methcathinone intoxication.

Main Methods:

  • Acute methcathinone toxicity was induced via intravenous infusion in conscious rats.
  • Dextrorphan was administered either as a pretreatment or immediately after the onset of convulsions.
  • Physiological responses including heart rate, body temperature, and survival were monitored.

Related Experiment Videos

Main Results:

  • Methcathinone administration led to tachycardia, hyperthermia, convulsions, and cardiorespiratory collapse.
  • Dextrorphan pretreatment significantly attenuated hyperthermia and tachycardia, and increased both convulsive and lethal doses of methcathinone.
  • Post-convulsion administration of dextrorphan reduced hyperthermic and tachycardic responses but did not affect lethality.

Conclusions:

  • Blockade of excitatory amino acid receptors by dextrorphan effectively minimizes acute methcathinone intoxication.
  • Dextrorphan demonstrates a protective effect against the physiological consequences of methcathinone toxicity.